Gene amplification in ductal carcinoma in situ of the breast.

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Gene amplification in ductal carcinoma in situ of the breast. / Burkhardt, Lia; Grob, Tobias; Hermann, I; Burandt, Eike Christian; Choschzick, Matthias; Jänicke, Fritz; Müller, Volkmar; Bokemeyer, Carsten; Simon, Ronald; Sauter, Guido; Wilczak, W; Lebeau, Annette.

In: BREAST CANCER RES TR, 2009.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

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Burkhardt L, Grob T, Hermann I, Burandt EC, Choschzick M, Jänicke F et al. Gene amplification in ductal carcinoma in situ of the breast. BREAST CANCER RES TR. 2009.

Bibtex

@article{8f2c64e7e48e4af6a44a6af78e548c4d,
title = "Gene amplification in ductal carcinoma in situ of the breast.",
abstract = "Multiple different biologically and clinically relevant genes are often amplified in invasive breast cancer, including HER2, ESR1, CCND1, and MYC. So far, little is known about their role in tumor progression. To investigate their significance for tumor invasion, we compared pure ductal carcinoma in situ (DCIS) and DCIS associated with invasive cancer with regard to the amplification of these genes. Fluorescence in situ hybridization (FISH) was performed on a tissue microarray containing samples from 130 pure DCIS and 159 DCIS associated with invasive breast cancer. Of the latter patients, we analyzed the intraductal and invasive components separately. In addition, lymph node metastases of 23 patients with invasive carcinoma were included. Amplification rates of pure DCIS and DCIS associated with invasive cancer did not differ significantly (pure DCIS vs. DCIS associated with invasive cancer: HER2 22.7 vs. 24.2%, ESR1 19.0 vs. 24.1%, CCND1 10.0 vs. 14.8%, MYC 11.8 vs. 6.5%; P > 0.05). Furthermore, we observed a high concordance of the amplification status for all genes if in situ and invasive carcinoma of individual patients were compared. This applied also to the corresponding lymph node metastases. Our results indicate no significant differences between the gene amplification status of DCIS and invasive breast cancer concerning HER2, ESR1, CCND1, and MYC. Therefore, our data suggest an early role of all analyzed gene amplifications in breast cancer development but not in the initiation of invasive tumor growth.",
author = "Lia Burkhardt and Tobias Grob and I Hermann and Burandt, {Eike Christian} and Matthias Choschzick and Fritz J{\"a}nicke and Volkmar M{\"u}ller and Carsten Bokemeyer and Ronald Simon and Guido Sauter and W Wilczak and Annette Lebeau",
year = "2009",
language = "Deutsch",
journal = "BREAST CANCER RES TR",
issn = "0167-6806",
publisher = "Springer New York",

}

RIS

TY - JOUR

T1 - Gene amplification in ductal carcinoma in situ of the breast.

AU - Burkhardt, Lia

AU - Grob, Tobias

AU - Hermann, I

AU - Burandt, Eike Christian

AU - Choschzick, Matthias

AU - Jänicke, Fritz

AU - Müller, Volkmar

AU - Bokemeyer, Carsten

AU - Simon, Ronald

AU - Sauter, Guido

AU - Wilczak, W

AU - Lebeau, Annette

PY - 2009

Y1 - 2009

N2 - Multiple different biologically and clinically relevant genes are often amplified in invasive breast cancer, including HER2, ESR1, CCND1, and MYC. So far, little is known about their role in tumor progression. To investigate their significance for tumor invasion, we compared pure ductal carcinoma in situ (DCIS) and DCIS associated with invasive cancer with regard to the amplification of these genes. Fluorescence in situ hybridization (FISH) was performed on a tissue microarray containing samples from 130 pure DCIS and 159 DCIS associated with invasive breast cancer. Of the latter patients, we analyzed the intraductal and invasive components separately. In addition, lymph node metastases of 23 patients with invasive carcinoma were included. Amplification rates of pure DCIS and DCIS associated with invasive cancer did not differ significantly (pure DCIS vs. DCIS associated with invasive cancer: HER2 22.7 vs. 24.2%, ESR1 19.0 vs. 24.1%, CCND1 10.0 vs. 14.8%, MYC 11.8 vs. 6.5%; P > 0.05). Furthermore, we observed a high concordance of the amplification status for all genes if in situ and invasive carcinoma of individual patients were compared. This applied also to the corresponding lymph node metastases. Our results indicate no significant differences between the gene amplification status of DCIS and invasive breast cancer concerning HER2, ESR1, CCND1, and MYC. Therefore, our data suggest an early role of all analyzed gene amplifications in breast cancer development but not in the initiation of invasive tumor growth.

AB - Multiple different biologically and clinically relevant genes are often amplified in invasive breast cancer, including HER2, ESR1, CCND1, and MYC. So far, little is known about their role in tumor progression. To investigate their significance for tumor invasion, we compared pure ductal carcinoma in situ (DCIS) and DCIS associated with invasive cancer with regard to the amplification of these genes. Fluorescence in situ hybridization (FISH) was performed on a tissue microarray containing samples from 130 pure DCIS and 159 DCIS associated with invasive breast cancer. Of the latter patients, we analyzed the intraductal and invasive components separately. In addition, lymph node metastases of 23 patients with invasive carcinoma were included. Amplification rates of pure DCIS and DCIS associated with invasive cancer did not differ significantly (pure DCIS vs. DCIS associated with invasive cancer: HER2 22.7 vs. 24.2%, ESR1 19.0 vs. 24.1%, CCND1 10.0 vs. 14.8%, MYC 11.8 vs. 6.5%; P > 0.05). Furthermore, we observed a high concordance of the amplification status for all genes if in situ and invasive carcinoma of individual patients were compared. This applied also to the corresponding lymph node metastases. Our results indicate no significant differences between the gene amplification status of DCIS and invasive breast cancer concerning HER2, ESR1, CCND1, and MYC. Therefore, our data suggest an early role of all analyzed gene amplifications in breast cancer development but not in the initiation of invasive tumor growth.

M3 - SCORING: Zeitschriftenaufsatz

JO - BREAST CANCER RES TR

JF - BREAST CANCER RES TR

SN - 0167-6806

ER -